PD, primarily caused by selective degeneration of midbrain dopamine (mDA) neurons, is the most prevalent movement disorder, affecting 1-2% of the global population over the age of 651-3. Currently available pharmacological treatments (e.g., L-DOPA) are largely symptomatic and lose their efficacy over time, with accompanying severe side effects such as dyskinesia. Thus, there is an unmet clinical need to develop mechanism-based and/or disease-modifying treatments2,3. The orphan nuclear receptor Nurr1 (also known as NR4A2) is essential not only for development and maintenance of mDA neurons4-7 but also for their protection from inflammation-induced death8. Furthermore, previous studies showed decreased Nurr1 expression in postmortem brains of PD patients9 and functional mutant forms in rare familial PD cases10, strongly suggesting that Nurr1 is a promising target for the development of novel disease-modifying therapeutics for PD11. Thus, there is a need in the art for agonists of Nurr1.